Evidence map›Paper›PMID 31247448›Full record

ArticleiScience2019

Chemogenetic Activation of Prefrontal Cortex in Shank3-Deficient Mice Ameliorates Social Deficits, NMDAR Hypofunction, and Sgk2 Downregulation.

Luye Qin, Kaijie Ma, Zhen Yan

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 46 citations in OpenAlex.

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  4. The role of the prelimbic cortex to nucleus accumbens core projection in the reinstatement of cocaine-seeking after cocaine-alcohol polysubstance use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Luye QinDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, NY 14214, USA.
Kaijie MaDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, NY 14214, USA.
Zhen YanDepartment of Physiology and Biophysics, State University of New York at Buffalo, School of Medicine and Biomedical Sciences, Buffalo, NY 14214, USA. Electronic address: zhenyan@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

Physiological and Pathophysiological Basis of StressR01MH108842 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YAN, ZHEN · 2015 to 2019
$2.0M
Functions of D4 Dopamine Receptors in Prefrontal CortexR01DA037618 · NIDA · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YAN, ZHEN · 2014 to 2018
$1.7M
Discovery of Novel Drugs for AutismR41MH112237 · NIMH · ASDDR, LLC · PI YAN, ZHEN · 2017 to 2018
$771k
Chemicogenetic rescue of autism-like social deficits in Shank3-deficient miceR03MH116453 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI QIN, LUYE · 2018 to 2019
$160k
NIDA NIH HHS R01 DA037618NIMH NIH HHS R01 MH108842NIMH NIH HHS R03 MH116453NIMH NIH HHS R41 MH112237
6 · The paper itself

Abstract

Haploinsufficiency of the SHANK3 gene is causally linked to autism spectrum disorders (ASDs) in human genetic studies. Here we found that chemogenetic activation of pyramidal neurons in the prefrontal cortex (PFC) of Shank3-deficient mice with the hM3D (Gq) DREADD restored social preference behaviors and elevated glutamatergic synaptic function in PFC. Moreover, the expression of Sgk2 (serum- and glucocorticoid-inducible kinase 2), a member of the Sgk family, which plays a key role in regulating the membrane trafficking of glutamate receptors, was diminished by Shank3 deficiency and rescued by Gq DREADD activation of PFC. Blocking Sgk function in Shank3-deficient mice prevented Gq DREADD from rescuing social and synaptic deficits, whereas blocking Sgk function in wild-type mice led to the attenuation of PFC glutamatergic signaling and the induction of autism-like social deficits. These results have provided a potential circuit intervention and molecular target for autism treatment.

Indexed as

Behavioral NeuroscienceCellular NeuroscienceMolecular NeuroscienceNeuroscience

Identifiers

PMID31247448
PMCPMC6599088
OpenAlexW2950529121

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.